Abstract
Sencar mice demonstrate an unusual sensitivity to epidermal carcinogenesis by initiation-promotion or single high-dose exposure to ultraviolet radiation (UVR). These mice exhibited an exaggerated and persistent epidermal hyperplasia in response to tissue damage caused by UVR. The persistent hyperplasia was not present in similarly treated BALB/c mice, a strain that is relatively resistant to skin carcinogenesis by initiation-promotion or single-exposure UVR. Epithelial cell proliferation and migration were examined by autoradiography to determine the cellular basis for the persistence of hyperplasia in Sencar mouse skin. Twelve weeks after irradiation, the rate of epidermal basal cell proliferation was approximately 4 times greater in Sencar mice than in BALB/c mice, whereas epidermal cell transit times were similar in the two strains. This result indicated that persistent hyperplasia was due to sustained epithelial cell division rather than delayed cell maturation. Surgical incision of Sencar skin did not cause abnormal hyperplasia, nor did this procedure enhance the induction of tumors by UVR. These findings suggest that Sencar mice may possess a heritable defect that mediates both tissue regeneration and tumorigenesis in UV-irradiated skin.
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